The biogenic amine noradrenaline (NA) can initiate and/or modulate motor activity in a variety of vertebrate species, including hatchling tadpoles of the European common frog, Rana temporaria (McDearmid & Sillar, 1997) and the South African clawed frog, Xenopus laevis (McDearmid et al. 1997), respectively. NA acts via a combination of both α- and β-receptor activation in Xenopus (Fischer et al. 2001), but the pharmacology underlying the noradrenergic response in Rana is inconclusive. When deprived of descending inputs following spinalisation, Rana embryos at stage 20 (Gosner et al. 1960) do not produce spontaneous motor activity as they normally do and the bath application of NA also does not elicit the non-rhythmic activity described in intact preparations. However, NA can initiate a transient episode of rhythmic swimming activity. Additionally, in the presence of NA electrical skin stimulation consistently elicits fictive swimming activity (N = 10), but only during a short period of time (ca 5-10 min) after which a 5-10 min rest is necessary before swimming can be initiated again. This noradrenergic response in spinalised preparations was blocked by the pre-application of phentolamine (40-50 µM; N = 5), but not by the broad-spectrum β-receptor antagonist, propranolol (40-50 µM; N = 8). Furthermore, bath application of the α1-receptor agonist, phenylephrine (150-200 µM; N = 7) could mimic the noradrenergic response, while the α₂-receptor agonist clonidine could not (150-200 µM; N = 4). Experiments in intact preparations show that co-application of phentolamine (50 µM) and propranolol (50 µM) blocked the response to NA (N = 2), while application of either antagonist alone could not. These data indicate that: (1) α₁ receptors are located on spinal neurons where they play an important permissive role in the generation of the swimming rhythm; and (2) the noradrenergic response elicited in intact animals involves co-activation of α and β receptors.

This work was funded by The Wellcome Trust.